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amazing. Thank you. Um, great food server that. Yeah. Thanks for joining us, everybody. So, like I said, today's the case 11 or diabetes, Your reason session. So I'm gonna be going over the basic anatomy and physiology of diabetes and the basic description of the types of diabetes and things you need to know on that face on different obese gonna go over acute complications of diabetes as well as management. We've desire to trial doing SP a little differently. Dissection. So instead of having them interspersed or at the end, I'm gonna have them all at the beginning. On day, we've got about seven or eight s to be a A on. But, um, we'll give them again to you at the end with the answers After two weeks presentation on, we'll see if you guys have more of you know, the answers at that point, um, the questions, hopefully, based on our teaching on well, explained the answers of the end of Well, so we start with the first one. I'm how it'll happen. I'm happy to launch the pull myself. Give me a second. So I think it shows you all of the questions. Um, when I launched the pool, but I'm gonna change the slides every, like, 30 seconds. Okay. Okay. That already can't answer them. Toby and I would hopefully cover all of all of this in our lectures, and we'll explain the answer. The end it is. Well, can you guys see the pool? Haven't going responses on the yet Know many responses yet, but that's probably because people are doing all the questions. No, no. For enough your abs. Yeah, but you can see all the Sorry about that, guys. I'm going to go back either. As you can see all the answers, I go back to the first one. Yeah. Okay. I'm gonna go to the third one. Yeah, yeah, yeah, yeah. On the fourth one, fifth one. Oh, yeah. Are sorry, guys would appreciate if you'd annotate on the screen. Thank you. Yes, on the sixth one. So yeah, seventh one, they're eight in total, by the way. Yeah. Yeah, and I'm gonna go to the last one now. Oh. Oh, that is the last one about Okay. Amazing. So you guys in somebody answers, That would be awesome. Can you see the answers? And three, it was just me you can see them get story. Okay, Go up 35% off the answers is any question. You want me to quickly go back to him? Happy to do that. I work with clear. If not, that's fine, too. Got 40% my way for about 50%. That's okay. Well, yeah, yeah, she's a good picture. Okay, It's still about 40%. And did you go back to question five and seven? Yeah. Okay. Um, this is question seven. Somebody you asked. Andre. Okay, this is question five. Um, someone else. A question, too, is well, which is this one? Okay. Can get if you Miss Aikens, for we stop. Okay, Amazing. Thanks for your answers. Gatti's. Let's look at that. I was going to get of pictures of these polls so I can cross reference than later so we can see how everything is improved at the end, properly helping out the other way around. Um, okay. Okay. All right. Amazing. Thanks. Everyone got with pictures on, but then we can start with the session. Great. Like I said, if you take her to the end was really answers, the FDA is and explain them well, right? So when we talk about diabetes, here's only recovering today in my bit. With the presentation, um, we're gonna be going over the basic physiology of insulin on how it synthesized Onda, how it works in the body. We're going to quickly go over a bit of metabolic metabolic signs on day, how the body is in the Fed and fasted state. I will describe the main types of diabetes you need to know, and the main like high yield point about them that you should probably know Onda also a bit about investigations and diagnostics. What kind of test to use when Andre What? The numbers are on values that you should know for diabetes diagnosis. So they begin ways the physiology of insulin. Um, it all starts in the pancreas. That is the most important organ that were involved with today. So it's this lumpy little organ that sits behind your duodenum on Do it basically has two functions. It one, as you know, a secret insulin that is endocrine function. It also secretes other hormones like glucagon and somatic statin on ghrelin. But what's important to note is that insulin secreted by beater cells on glucagon is secreted by alpha cells. Both alpha cells and beater cells are types of islets of longer hands, and this is like a key word. You probably heard of it before. It's it's funny because insulin glucagon are opposites. So, um, as we learn on, they have opposite functions in terms of the exocrine function of the pancreas. Here, the pancreas had these asking ourselves and ducks, as you can see in the image over here, where all these cells secrete enzymes like hydrolytic enzymes secreted into the middle, which then collects into a duct and then secreted out of the pancreas in pancreatic juice on D. Actually, this makes up 90% of the pancreas dysfunction. Um, where is the end of coin is is about 10%. So those are the main functions. Pancreas, Um, and we're concerned with the end of crying part of it today. So how is incident synthesized? How was it made? It's made like any other protein in the body, so it goes through the process off mRNA, a transcription. So what happens is there's a gene that's an insulin gene that stimulated and stimulations insulin gene causes transcription and translation off the incident proteins than put together to make what's called pre pro insulin. Okay, that's your first product in the process. As you can see, Preprotein still in has little blue colored tile on the edge. This blue color tile is then removed. It's called a signal sequence. This signal sequence is removed to give you what's called Pro Incident. And then finally, you get, like the formation of these disulfiram bridges on, and you get further cleavage off this to produce what's called proinsulin. So it's called Insulin Doesn't Care Over there, that is insulin. Now what happens when you produce? This is when you Cleve pro insulin to insulin and something else that something else is called Cpeptide. And that's what Cpeptide is. It comes from the synthesis of of insulin, so initially appropriate for insulin, which is cleaved to pro insulin by removing single peptide, which is then cleaved into insulin on CPAP tied. And the reason we use the reason it's important to know that CPAP side is also cleaved is because because they cleaned into equal concentrations. If you want to know how much insulin someone is endogenous Lee producing, if you look at the C peptide levels. That's a good indicator. If someone has a low C peptide level, that means that they're not producing that much endogenous insulin because the amount of CPAP tight should be proportional to the amount of insulin in the body. If, for example, someone comes in with an episode off hypoglycemia and then you decent bloods and it shows you that the CPAP side is high, that's telling you, for example, that they haven't insulinomas or something. Where they have an excess of insulin in the body on this is causing them to be hypoglycemic, as indicated by the C peptide. I hope that make sense. So I was insulin secreted. Well, the main trigger for the secretion of insulin is the fact that glucose is not present in the body after meal. Right. So the presence of glucose and the uptake off this glucose why are glued to transporters in the pancreas will stimulate the initial secretion off insulin. And this is, as you can see, the biggest co. So we started the beginning of this girl. At the bottom is when you have a little glucose ingested and then when this is up taken by the glue two transporters in your pancreas, and your beater sells this initially like triggers this giant spike of insulin release, which is over here. But then, usually the insulin is not enough toe break Teo work for all of the food that's there, and therefore you need more insulin, and you have to kind of synthesize this and trigger of senses off this. So the first place is increased. Secretion is insulin that's already there in the B cells. On the second phase, which is like a smaller release is when news new incident is synthesized and released. I hope that make sense. Onda. The most very important thing to remember is the mechanism of action action of insulin. You could go into detail about how exactly it works, but the most important thing I remember is that insulin acts on piracy. In kind is insulin. Receptors are tyrosine kinase type receptors, which means they dimer I've lost, violate and all that stuff, you know, under PCs about how it ties in kind of receptors work incident receptor, the ties in kind of receptors that's could be a very common STD, a question where they kind of, um, describe what kind of receptor it it is. And then they ask you what it is, and you're like, Oh, it it works for glucose on do it's tires and kinda, is that it must be an incident receptor. Help make sense. We then move onto bit of metabolic science. Um, that's about the Fed and fasted states. So in the Fed state is this is the state after you eat into this is wiser to four hours after you've just had a meal on Do. The main thing to remember in the Fed States is that your body is trying to take all this food you just eaten, unlike store it. So you have all these. Your resource is floating around and you find a way to store them. And that's exactly what's gonna happen so well, it's gonna happen in that state is that instead of breaking down glucose and breaking down fats, your liver is going to take all all the small bits of glucose and converted to glycogen, which is a bigger carbohydrate and easier to store. Instead of fatty acids floating around or broken down fatty acids, it's going to take any fatty acids in your diet on D build them up into little bigger lipids for storage. Similarly, in your adipose tissue is indicated by these yellow globulin. You haven't increased uptake of fatty acids that they can be converted to lipids on a down, regulation off like policies, which is the breakdown fat and again in your muscle. After a meal, you have the up regulation off gluten four transporters that transport glucose and as well you have the again do the conversion of clock glucose to glycogen for storage as well as protein synthesis. In these posters, you can see that the breakdown of substances on the metal on breakdown of them to energy is usually not happening. For example, clock in General Isis, which is a breakdown blockage interview Coast is not happening because you're trying to do the exact opposite, and you're trying to story of food, not break it down. But let's say in the opposite scenario, you haven't eaten in about like 15, 16 hours. It's been a while. You haven't eaten anything, and now your body. It's not getting any new stores and therefore has to rely on it's existing stores to give you energy on the world's gonna do that is is gonna work in the exact opposite mechanism off what we just saw on the left. So in the liver, for example, instead of seeing in upregulation off things that build up like a gyn and build up fat, you're gonna see process that breakdown glycogen and break down fat. So to give you the energy you need to provide yourselves with energy to work and to survive, So it's literally like the exact opposite. It's pretty much a mirror image. Um, as you can see, that's the main difference between the Fed and the frosted states. Okay, I just question someone's asked, How is the increased fatty acid uptake but decreased like policies? You have increased fatty acid uptake because that is the function of your adipose tissue. Your adipose tissue is not directly connected to your gut, and therefore fatty acids don't just diffuse into your adipose tissue automatically. Adipose tissue has to make the effort to firstly object this party acids and then convert them into lipids within the adipose tissue to get like a genesis on do um, fatty acid uptake. And there's a down regulation, my policies, same sense. Great. So how does insulin work and where does it work? So this insulin has the world we usually look at? It is like you said, it's an incident just with Blue Coast and nothing else. Well, the truth is, insulin has metabolic effects on every macromolecule in your body. I mean most types, so obviously has faxed on carbohydrates like Google's. What it does is that after eating a meal, you have a release of insulin on. This is going to upregulation presence of glute for transporters on your muscle and adipose tissue membranes on this Means is going to be an increased uptake of blue goes into these issues to encourage the up uptake and storage off these resources again. It's going to stimulate glycogenesis in the liver. You want to store the glucose, the glycogen, and it's going to inhibit the opposite processes. And the net effect is that it's going to help lower your blood glucose by kind of shoving everything out of the blood and into issues on fat. It's like we saw earlier insulin kind of support of the process off lipids, and this is on converting fatty acids toe bigger lipids that are easier to store and inhibits the opposite processes you can see in terms of proteins like we saw in the muscle. Not only does it up regulate glutes were friends borders, but it also stimulates proteins. And this is so It kind of simulates the uptake off amino acids, which is the, you know, the building blocks of proteins on. Then build them up into protein cysto any muscle and inhibits the opposite process, just like we still earlier. And finally, it also has an affect on potassium. So on insulin release can basically, um, release potassium from the cells into your blood. Um, Onda so does the exact opposite. What it does is that it shot for calcium into your cells. On application of this would be in DKA as Toby talk about later on, I'll let him talk about why it's important. Um, but yeah, So I had mentioned a couple of glucose transporters I'd mentioned you to include for and this is just draft table I found online. That very nice see, summarize is on all the glue. Transport isn't exactly what you need to know about them. So when you come, can you concerned you transporters on the lot of details you could learn about them like some of them only transport glucose in one direction. Some of them do it in both directions. Some of them have high affinity for glucose, etcetera. But the main thing I want to talk about here today is that the km value is a value that describes, um, how easily the channel is going to accept Blue Cross through the membrane so it's inversely proportional to finish he. So there's a high can value. That means that that channel has a low affinity for glucose. That means that it doesn't like glucose as much, and it's going to take a lot more blue coasts. Ah, much higher concentration of glucose allow that channel to open, so that usually happens in your liver, your pancreas you got on your kidneys. These are tissues that usually metabolic eyes, insulin after a meal like we discussed earlier on both of these blue two channels only open at high concentrations of glucose. Conversely, you have blue three channels that open and very low concentrations of glucose. This means that they have a high affinity for glucose, which means they open really easily. And as you can imagine, the tissues that require a lot of glucose. All the time are gonna be the ones that will have a very high affinity for Blue Cross transporters. So, for example, your brain, which is on which is switched on all the time up placenta, which is sending nutrients to your the fetus. He's so really vital for your survival and general function, and therefore they need a high affinity for glucose to be able to always have access to glucose. That makes sense. Girl thing, I notice, is that beautiful transporters that was on muscle adipocyte are into independent, which means that the presence of insulin can up regulate their presence. But there's also case where, for example, after exercise exercise also upregulation glute for transporters on That's just somebody itself is your physiological thing. And that's an insulin independent reaction. The nothing I'd say is that you know that gluten five transporters transport fructose so oh, yeah, finally, let's talk about diabetes. Let's talk about where insulin kind of goes wrong and where all of this stuff becomes pathological. There's many different types of diabetes you might have come across the last couple of weeks. I've just listed there over here. Um, I'm mainly gonna focus on top three trades presentation for the sacred time. Um, but if I don't have any questions later, I'm happy to answer them about the bottom three. So we start with type one diabetes. Um, can anyone tell me what's the root cause of the problem is in type one diabetes? Autoimmune? Yeah, sure, it's autoimmune, but, like, what's the problem? Someone said, beat a sat of destruction. Okay. What happens as a result of beautiful destruction? Lack of Internet? Yeah, perfect on. What happens if you don't have enough insulin? What is the what is the end result? Hyperglycemia. Exactly. That is essentially the entire physiology years. I would diabetes. Oh, the court. The core problem is what's called absolute insulin deficiency is when your beater cells are destroyed. Do 10 auto immune cause. And therefore there is no insulin being produced in your diabetes cells. So handle the blue coast. And this means that the glucose, after which you eat from your diet is not being metabolized properly. And as a result, you gotta build up because your blood, which we call hypoglycemia. So what are the what is easy? Older 51 diabetes. What can cause it? Well, there's some genetic associations, which h it with these HLA genes d are three and er four, but also associated with other other autoimmune conditions. This is often the case with most autoimmune condition is that if somebody has one autumn in conditions, the chances are that they probably have another one or the chance the risk of them developing another one is quite high on a pair to a normal person. So some of the like higher risk autoimmune conditions diabetes type one diabetes is associated with Hashimoto. Thyroid uh, parotitis see like disease on do primer Jalyn's efficiency. So what does it look like? Well, the key features you probably have learned time and time again, or your diabetes case in someone presented with diabetes the first time is feeling really thirsty. There were a lot more than usual on D. They are just drinking a lot more water and and things like that on. In the case of Type one, diabetes that probably lost some weight as well. On the appearance is usually quite thin. Things generalization. But it is one of the typical signs because in order, immune disease it can develop early on and therefore has a quite a girly onset before the age of 20 years old, usually on and sometimes because, um, because some people don't realize that they have it, it can get really bad to the extent where they develop complications like DKA, which is diabetes. Ketoacidosis on that can often manifest as the first presentation off dive. One diabetes, um, on other common presentations with type of diabetes is things like visual disturbances, because what happens is when you have hypoglycemia. And this can mess up, mess with the automatic balance off the lens in your eye and therefore can cause, um, blurry vision. Basically on do alter. Just fatigue on be poor wound healing. It's just stuff signed you'd see on them when they turn up. So what kind of things? What kind of test would you run? Tow Look to investigate someone who you suspect has Type one diabetes? Well, firstly, obviously you'd run some tests to look at that blood glucose, and there's different types of tests you can run that we'll talk about in a bit on. These will tell you first of all the the hypoglycemia hypoglycemic on the extent of the hypoglycemia as well. If they have a low C peptides, Um, just cause I want to know if people understood that, can someone tell me why a low C peptide would indicates that someone may have type one diabetes? It's not diagnostic, but it is. It does. It does help his corroborative. It's endogenous. Exactly. So if someone is not producing insulin, they're not producing CPAP side either. And therefore they might have a low C peptide. Yeah, and because of diabetes is also immune disorder. That gonna have there are gonna have 80% of patients have some auto antibodies detectable in their blood. These will be anti G A D and anti. I see a antibodies or two antibodies, and additionally, you can also do some urinalysis to look for glucose in the blood key tone as well as proteins. If you look, if you're looking for microalbumin, you at micro albumin here urea, which is protein in the blood. I mean looking for kidney function to see how well the kid is doing. That's type one diabetes now with Type two diabetes. What's happening is that you can have one of two problems one is that you're having a problem with the secretion off insulin itself from the Beatles cells. Oh, are you having or your PSA creating the insulin? But your tissues in the body are not responding to it, so as a result, you get what's called insulin resistance. And this means that that your tissues are not up like multiple eyes and glucose, and as a result, you're getting a buildup of glucose in your blood. So how does this happen? On be wise, like houses become a bad thing. Well, what happens in Type one diabetes, like we talked about, is that there is no insulin to begin with. How old Type two diabetes You do have insulin being produced on D, but what happens is that obviously your tissues aren't responding. That's why I explained, and as a result, you could hypoglycemia. What's gonna happen is that because there's so much glucose in your blood, your brain is like okay, there's so much glucose. I need to continue producing more and more insulin toe, beat the glucose and get it back down because your brain doesn't quite realize that your tissues are resistant and not responding so as a result you're beat ourselves into over produce insulin, and this isn't going to help because this is actually has no effect of you close and they're going over. Get overworks the extent that they die get damaged Onda. Finally, you get a point where your incident secretion itself is dysfunctional and therefore you get the problem of incident secretion dysfunction. So Type two diabetes can be a mix of both, basically. So let's talk about, um, the etiology type of diabetes. Um, it's very, very, very strong correlation with other cardiovascular risk factors, like a metabolic syndrome and central obesity, uh, also very strong risk factors of family history. Fabulous Bt's If someone is prediabetic, we'll talk about what that is in a minute. If someone has a history of gestational diabetes, which is where if they had diabetes Type two when they were pregnant, when you don't really have auto antibodies anyway, that here because it's starting autoimmune disorder in terms of how they present again, you get a typical diabetic symptoms, which is polyuria polydipsia. But sometimes, instead of seeing patients that are saying, you might see patients that are overweight because of the correlation with cardiovascular risk factors. That's one difference in clinical presentation with type one diabetes. The arms that is gradually happens over time. It's not. Snow happens overnight and presents, like extremely cutely, Really early people usually present in, like forties, fifties or even older than that. Um, and you will have similar, um, things like our blood vision and fatigue and poor wound healing on there. Some skin signs that, uh, um there are signs off incident resistance. These are our condolences. Nigra cans and be nine like Accordions. And these are basically is, like, these dark think pigmented regions on skin, especially in your skin. Folds on that are not diagnostic of anything, but it just assigned off things like incident resistance. Um uh, yeah, but in terms of diagnostics, you've got a very similar thing. What we do in type one diabetes. But you do glucose tests, blood tests. You look for the C peptide, which doesn't not usually very helpful in this. Um Onda. Also, from your analysis to up before I move, I'm going to see that he questions in the chaps. Ah, okay. In terms off gestational diabetes, this is when you have develop type two diabetes where you are pregnant. Um, anyone Tell me, Um, okay, I would stop. I say that in the state of pregnancy, you know, actually, physiologically developed into the resistance within the body, and this is normal. Can anyone tell me why this happens? So try to find the chaps going books? Uh, no, no, no. It's all that anyone Tell me why you develop. Why would you do? Yeah, but yes, I do is impossible. The child. Yeah, that's that is the purpose of developing into resistance. But anyone tell me how incident resistance develops in pregnancy in the first place. HPLC. Yeah, exactly. HBO is, um ah, hormone secreted by your uterus during pregnancy contributed by your placenta during pregnancy. It's called human placental lactogen. And this induces internal resistance in the body. And this is actually really good because you have this new human being developed. You have this new human being being developed within within another you and being, And therefore the net glucose requirement is a lot higher than just for one human and therefore a lot of blue cause needs to be redirected to the fetus. That's what happened here. But what happens in gestation diabetes. When is when this kind of gets to elevated in extent? Words like bad and dangerous. So what can happen is that it gets the hypoglycemia where the insulin resistance in the mother's body gets so bad that the Beatles cells are no longer over able to cope and able to maintain normal class EMEA in the blood. And this leads so build up of Lucas, the blood lead the hyperglycemia. And this can have adverse effects of both the mother on the child and also has effects on the future outcomes off the child as well. Some risk factors for developing gestational diabetes for the mother is generally if she, um, has metabolic syndrome. Is has a B. M I over 30 if she's had a previous child that was quite large on birth, Uh, if she has polycystic ovarian syndrome or she has multiple gestation that she's she's been pregnant a couple of times. The adverse effects have have effects on both the fetus on gum, other as well. The most important one, I would note that comes up in SBA is is that this can result in a high risk off, um, like interrupting the birth of the fetus. So in terms of in part relation itself, what can what can happen is the fetus can develop what's called shoulder dystocia as a result, because the fetus is macrosomia gets too big on this can cause complications. Um, for mother on having gestation Diabetes can increase the risk of things like preeclampsia with Onda, therefore predispose you to things like a clamp. See out where you get seizures and things, and that can be quite fatal and deadly. Um, there are also many a second because the diabetes So we've doctor by the primary cause of diabetes, family history and things. But there are You can have other medical conditions in your body, or you could be taking certain medication that can cause you to have diabetes. For example, the most common one you might see on the ward's is someone who has pushing syndrome, which is basically cortical like glucocorticoids induced diabetes, where someone's taking too many boogers corticoid for immunosuppression or something on Do this is causing them to develop diabetes, like developed too much glucose level. Finally gonna move onto the investigations and diagnosis bits in more detail than talked about earlier. So in terms off the different blood glucose test you can do. There are four different tests you can do. Two of them are fairly similar and that their readings will be interpreted the same way. And these two are random glucose and oh, G T t. So random glucose is when someone comes into the GI Clinic or someone comes in to the any on Do you take their blood glucose any time of the day? It is a matter of the eating on anything. I'm just is a random little around. And glucose, can someone tell me what your GI T T stands for? Yeah, old Lucas. Or is this exactly? Yeah. So this is when someone comes in to the clinic. Usually when they're suspect of having gestation diabetes, you give them a girl 75 g dose of glucose, just straight glucose. And then you measure that blood glucose at at the time that you give it to them, said zero hours and then again two hours later and you're basically looking at the ability, the ability off their body, and they beat ourselves to deal with this increased load of insulin. You then have a fasting glucose test, which is when somebody generally has not anything to eat for at least eight hours. So it's most community to do this test in the morning to someone can, like, come in before they have their breakfast, and they haven't eaten since dinner. Um, and this is called the fasting glucose test and this season whether their body was able to deal with the last dose of insulin. But they're the last two hours of food that they had the night before. And then finally, you have your HBA one C test that, uh, is a measure off the amount of glycated hemoglobin. What is like a C hemoglobin? Basically, when you have hypoglycemia, excess amount of glucose can have oxidative effects on him. A globin. This can change the configuration of a hemoglobin, which is a protein. Onda cause it to become what's called glycated hemoglobin, which is bad, which is dysfunctional and doesn't function like normal hemoglobin and therefore is an indicator off someone the extent of somebody's diabetes. Um, the reason it can only be done every three months is because hemoglobin, of course, is found in red blood cells and red blood cells turn over every three months. So if you do one today and you do one next week, you're going to get pretty much the same reading because you have the same red blood cells in your body. Whereas if you do it three months or four months from now, likelihood is that somebody has had a turnover off the red blood cells. And therefore you get a revised reading off that HB a one c glucose control can. Someone told me the chapped when you shouldn't be using HBA one C, which looks like a t o assess somebody's blood glucose type one diabetes. Yeah, type one diabetes. Yet because the amount of insulin sickle cell anemia. Exactly. Because media, your red blood cells, hemoglobin is distorted anyway. Yeah, amazing. Yeah, really good guys at the end of my slides. At the very end, I have a whole list off off situations where you shouldn't be using, um, HBO, HBO and see to make any kind of diagnoses for patient on. You can look at that when you get this lights, but the purpose of time I won't go over that now, So let's talk about the values you need to know for diagnosis. So, um, when family comes in and you do a blood test, um, you do a random glucose tester or GT basically because you're just giving them because you expect that Lupus to be on the higher side when I say higher side, I'm saying, like above. Eight above. Nine. On pathologically it's above 11.1, which is the official guideline value. So somebody comes in and you could do about, um, Blue Cross, and it's above 11.1 or sound of you. Ask someone to come in early in the morning before breakfast. You can go fasting. Glucose on this is above seven. Um, then this is indicative off the inability to deal with leukosis in their body and therefore diabetes cause they have hypoglycemia. If you do an HBA one c and again, it's above 48 millimeters Come, all this is again indicated off. Ah, hypoglycemia That's been there for a while, Onda. Other investigations you can do, of course, our Cpeptide autoantibodies that we talked about earlier. But the diagnostic values of these so you can have either a random glucose probably goes or or GT or fasten comma glucose for diagnosis with Type two diabetes, it's pretty much the same. Um, the exactly the same values. You should remember that one important point is that if someone's come in complaining about, some other symptoms are unrelated to diabetes, and the common would like a headache on bats to do with that migrant or something. And you do a blood glucose anyway. And it's an incidental finding that that blood glucose is high. That is not sufficient to diagnose them with diabetes, because that could just be an incidental finding. It could just be that day because they're not symptomatic. Therefore, if somebody is asymptomatic on that drug because is high, then you have to repeat the glucose test on the separate occasions. Ask him to come back a week from now something. Repeat the tests. If they're bad, Lucas is still high. Then. Then you could make a diagnosis of diabetes if they're symptomatic and they come in complaining of politics, see a polyuria weight loss, things like that. What I want, for example, then one reading. Is it sufficient to make a diagnosis that's okay? Like pre diabetes, pre diabetes is kind of the awkward stage between when your body is not quite normal. Your blood glucose is a little high side, but it's not high enough to be diagnosed as diabetic. So there are two types off impaired glucose regulation that make up prediabetes. One is when you have impact fasting glucose. So after a meal, for example, your body's not able to tolerate because you just eat and and deal with it and metal it after a meal and the other is impaired glucose tolerance. It sounds similar, but basically this means that your tissues, your external tissue around your body, like your muscle on your Adipost are unable to deal with. The glucose has been released into the blood after meal, so we need to remember that is that impaired fasting glucose associated with hepatic resistance, where as impaired glucose tolerance associated with like different issues like muscle and adipose and these patients are more likely to develop Type two diabetes and cardiovascular disease on, And these are just threshold values. You look yet prediabetes diagnosis. I'll let you go over this new one time. But as you can tell, for example, it's kind of in the middle off being healthy and being diagnosed with full on diabetes. Great to the law. My slides. Thanks so much for listening. You have any questions? I'll be on the college if you put them on the chapped. But now I'm going to, uh, pass away to Toby. Thanks on. Uh, that was really great. I was just wondering, um I don't know how long Toby's presentation is. Would it be worth having a two minute break just to give people some time? Yeah, I go for it. That's a good idea. Okay. We'll come back at two minutes to eight. So you got about, um, five minutes, You guys, then. Okay. Thank you for that presentations. Hold it. By the way, that was really useful and really clear it going through all the pathophysiology. And the diagnosis is, well, diabetes. I know. I sent me recap a lot on Toby. You ready to go for a second part? Yeah. Yeah, I'm ready. Sky. I'm step my power point shot now. Yeah, Yeah. Okay. Yeah. Sorry about my name. Rita. It's just Yeah, actually, my drug we tried Oh, sorry. Yeah. Okay. Yeah. Right. Okay, so thanks so hard for giving that first half the talk to really set us up for diabetes. Now, in my section, I'm gonna be talking about the management and then the complications of type one and type two diabetes. So to start with, I just realized Reiterate, what's the Honda says on? So type one diabetes, you get damaged. Teo, your beater cells leading to insufficient insulin production on as a result of glucose can't be absorbed by cells in your body, so they're effectively being starved on. Instead, your body has spread down fat, which can produce high levels of key times. Okay, So can anyone tell me the main acute complication of type one diabetes? Just put it into the chop? No. Okay. Yeah. So DKA. It's the main complication that we worry about in type one diabetes on Diz often how patients first present on. So you're if you have insufficient is them production? You end up with extreme hypoglycemia as your body has no way to absorb this glucose. Since that your body carries out be truck station to metabolize fats to be used energy on in the form of key times. Now, ketone is convened harmful to the body because they're acidic. So you end up, um, in acidotic States and then a Hence the name ketoacidosis. And then here's some science and symptoms that dehydration, nausea, vomiting on mental status change. Um, acetone breath. So patients have a really distinctive smell to their breath. If they're in DKA and then also you get frequent urination. Um, and with frequent urination, this means that patients are often severely dehydrated when they have DKA. Uh, this is something so hard attached touched on with Theo. Effect of insulin on potassium. Now in the body, insulin causes potassium to be moved inside cells intracellular lee through sodium potassium ATPase. Now, if you don't have the insulin like in type one diabetes, you end up with high levels of potassium in the blood because no potassium is being moved into those cells have. And then you get low levels of potassium interested literally. So this means in your blood you have high levels of potassium which can lead to you every three years. Um and also you remember that I mentioned frequent urination. So when you urinate, you also lose a lot of this potassium in your blood. So even though it levels of potassium in your blood are high at the levels of potassium in your body over where actually decreased Because you're urinating that potassium from your body. Okay, so can anyone tell me the management that we might do for DKA? If you don't know, I just take a guess and put it in the shop. They're three steps that I'm going to mention. Yeah, Okay, so I'm seeing a lot of people saying fluids. Um, yeah, yeah, saline would be the first intervention we do because patients are really dehydrated, so it's important to get that fluid levels back up. I'm also seeing a lot of people are saying insulin, so yeah, obviously, on in patients with type one diabetes, they're not producing insulin. So that's the main problem. And that's what we need to fix on. I also added that you can get extras infusions, So if your glucose drops to below 15 and minimal people eater because of the incident infusion, you can then add dextrose to make sure your blood glucose doesn't drop and you felt or dangerously like I should say okay, and then the last one, some some of you got it. ISS potassium infusion. So this doesn't always happen, but in patients where the over batasan has decreased. Then you can get severe hypokalemia because you give the patient insulin. And this causes the potassium to move inside cells from the blood, which will lower the potassium in the blood. It could be dangerous for patients. So that's why we give them potassium infusions. His, um, management of type one diabetes that grade three. Now, I I mentioned education. One of those is a diet with low blood scenic index foods. Can anyone give me some examples of foods which might have a low glycemia connects? Yeah, I screamed. Okay. Ice. Yeah. So vegetables really get, um, whole wheat? Yeah. Yeah. This is already good stuff. So glad, um, foods for the localized in the conduct of foods that, um Where it takes a while for your blood glucose to increase after eating these foods. So vegetables in any whole grains, like cereals. Lot of people said whole meal on. So foods you might want to avoid would be back. Any sweet food? Um, white rice on D on foods will cause your glucose to spike. Yeah, on. Then. I just have someone mentioned alcohol in the chat. I did mention care about drinking alcohol on because you can cause hypoglycemia than like Lauren says. You can also get hyperglycemia. Um, so just with alcohol causing fluctuation in your blood glucose level was, um it's important. Teo, be careful. Winter calcar. So here's an insulin therapies on insulin pumps will monitor your blood. Glucose is constantly on d them. Release insulin in response to what the glucose is. So this will use rapid acting insulin, so you can almost respond immediately to whatever your blood bleed. Case is to try and keep this constant as you can. Um, then you also have your strong acting insulin Rapid on long acting on the first line treatment is to combine a a long acting insulin with a rapid active instant before meals. No blood glucose monitoring on something that's becoming really advanced recently on D. One way of doing it is the free laborers. So this is the device in the picture on the top, right, which monitors your blood glucose in your subcutaneous tissues on down. Um, you couldn't see what this is through a smartphone or other devices to get live updates and what your blue coast is, you might get alert if you're having a high pay, um on these are always accurate because it takes a while for your blood glucose. Teo the fuse and impact the glucose in your subcutaneous tissues. Um, and I put here the when you're driving, you should be finger prick tests on you. This is actually changed recently on D the D v l. A has said that you don't have to do your finger prick tests before driving. You can use your free liberal, but if you're having hypoglycemic symptoms, you should still do a finger prick Test sick day rules. Um, these quite literally the rules you should follow if you're sick. So when you're sick, your body releases more insulin from your liver to help fight the infection on health. This is good because you need the energy in your body. However, in diabetes, you went produce the insulin. In response to that glucose I saw I your body went up to absorb quickly case in your body. And patients may think that because their glucose is high, they don't want to eat or because they're not eating. They might not take that insulin. It puts them at a high risk of DKA, but instead, um, your body produces more insulin when your help, so you should actually increase your dose of insulin on patient should continue to eat because they need the energy to recover from the illness. But it's important to monitor month. You're back to your case, and I've mentioned that Type two diabetes you stopped taking metformin. And so, for now, your ears on the's. Just 22 diabetic drugs, Um, which compare some patients of risk. Um, off. I paid I Sr specifically Self Nigeria's. I'll talk about that later. Okay, So moving on to type two diabetes, this is when your body becomes tolerant into Then I think the harder spoke about this really well, so I skipped this line. Okay on. Did anyone tell me the main, um, thing that will be worried about more keeps Lee in Touch two diabetes. I guess you could say the type to your equivalent of DKA, but not literally. Yeah. Lots of people are saying hate. Hate us on there. Be completely right. So hypoglycemic hyposmolality syndrome. This used to be called hunk or hung syndrome. So I'm pleased everyone's used to correct a neurology that because it's now a crude hypoglycemic, hyper as medicine. Dream on. This is when on your type two diabetic with poor guy, seen it control. See, end up with extremely high degree that glucose on the high blood glucose pulls water into your urine. Causing dehydration because you have frequent urination is no the same pictures DKA because diesel produce insulin on some of it will work. So you don't end up with a key Tosis that we see in DKA but on you'd still have similar management. So fluids you might consider giving insulin onda possible pap potassium replacement therapy. And then again, the signs and symptoms similar, Um, you are at risk of, um, are cardio infarction on from the from Brought it complications because the extremely high Buckley case can make about thicker on. Increase your risk of a thrombus. Okay, so hypoglycemic complications. This could be seen in type one and type two diabetes on drink. Some patients. Some people think type one diabetes is court. When patients are a young onda. As a result, that treated on they won't be affected by the hypoglycemic complications. Been reality type one. Diabetic control isn't perfect on most patients. Do you still have a higher blood glucose? And they should. And they do experience and complications. These could be it divided into microvascular on macro back Spassky complications. So can anyone tell me some macrovascular complications off type of hyperglycemia? That's not quite vascular. What? Okay. Um, yes, it is. Someone said peripheral vascular disease. Some nurse has stroke. Um, someone said diabetic for come under. Diabetic. Um, cardiovascular retinopathy. Um, so I'll I'll explain it all in the next couple of slides. So maculate macrovascular complications. Um, like cerebral vascular disease. Like someone said, Strike Onda cardiovascular disease. Let's keep set em I and then get peripheral vascular disease such as peas. Just damage to blood vessels. Um, now I'm going to move on to talking about micro vascular complications on this is when some of your comments on diabetic foot retinopathy will come in. So when you have high levels of glucose in your blood, you end up on guess a hardening of blood vessels on in your kidneys. This hardening of blood vessels can prevent filtration through the gum. Areolas on his belly is causing the kidneys over work on a rou. Um, it causes your, um g fro lower Onda. In severe cases, you can end up getting on. Chronic kidney disease may be onto resting up with it so again on high blood glucose, good heart and blood vessels, and goes now ring on often in diabetes, especially type two. You might have high BP anyway, and this could be worsened on blood. Vessels could be damaged. And I've wrote this could lead to high pox here on. So as a result, you get things seen in your eye such as cotton wool spots, ahem, urges or new vessel formation specifically in new vessel formation. If this occurs, it shows that your eye needs more oxygen, more nutrients, and that's why it's forming the new vessels. So this is a particularly and late stage sign of severe hypoglycemia, um, out neuropathy. If you can get different sorts of neuropathy and hypoglycemia. An interesting one is autonomic neuropathy. So often people think of like nerves is feeling things obviously in, um, what's not mean? Your apathy. It controls your GI tract, um, a rectal dysfunction on there on your BP. So if that doesn't work, you can get gastro paresis when your GI tract might not move for your stomach Computed. I just food on erectile dysfunction or postural hypertension. You also get sent sensory neuropathy. Um, this is when diabetic foot comes into play. So and I said glove and stock stockings distribution. So on Bache inskin have reduced sensation and that peripheries and such as in their hands in their feet like a glove and stop stockings and distribution. I right, stop there should say it's it should say stocking. Um, I'm specifically in your feet. If you, um, would step on something normally would feel it on, Do you take whatever you stepped on out of your that anyone be an issue? But if you have a center in Europe, you might step on something and not realize. And then this could cause a small cut in your foot which eventually gets that larger. And then you might get ulcer. And then if that gets infected, then you could end up with and abscess on. But the abscess gets worse. Seeing that gangrenous foot, um, on you could end up getting, um, entirely going. Banquets fits, which might require some sort of amputation, perhaps of your toes or your entire fifth. So that's just how simple things such a Z neuropathy lied to you Damage have a cure for it. Now I know people mentioned peripheral vascular disease area. This makes the whole process a lot worse because if you have peripheral vascular disease, you might not get enough nutrients to your feet as well. So any infection you do have to take longer to heal. Yeah, and then just finish off Morning Europe. These that is a single nerve. Who's is That's your oculomotor have. This is just an more specific now might be affected. Eso. To avoid these complications, you get retinopathy screened every two years. Annual fit screens on, you know annual kidney function tests now for the management of type two diabetes say this is often, um, done through drugs. They can be, um, it should be in addition to lifestyle changes as well. Thank you. So I'm going to talk about the mechanism of insulin release. Um, just a recap, which so is release insulin. There's someone pretended into the chapped fetal cells. That's correct. So here I've drawn a lovely diagram off a beater cell, which shows glucose being up taken, but also these things called incretins, which up? Taken from your job tract And there are hormone. So when you eat, you get increased levels of glucose on incretins entering your reader cells. Uh, now, this causes an increase in the levels off ATP through, like Colaces. All right, on the ATP then acts on this potassium pump, which normally pumps potassium out of the cell. That, um when there's ATP within the cell actually causes the challenge close, causing an increase in potassium within the cell when there's high level was a potassium in cell causes depolarizations, which causes a voted gated calcium channel open, which will then cause vesicles containing insulin to move, um, to the cell membrane and be released. No type two diabetic drugs act on this whole process in a lot of ways. Yeah, you the our keys. Okay, I just lost my mouse for a moment. Okay, So the first drug I'm going to talk about is on incretins mimetic. So I speak incretins on. It's a hormone released when your body consumes food on is likely coast in accent in, always on the beater cells. They also increases satiety. Um, yes, I incredible Matics. Such a Z exenatide just actor amplify the whole process on because increase insulin release to lower blood glucose gliptin also take advantage of the system. So return here s o saxagliptin, for example. Um so if you look down here, I've written on a DPP four DPP four axon incretins to inhibit them, but it's normally would cause reduce insulin release on this word back to regulate insulin release. However, we want more, it's limitless. Therefore, we have gliptin which inhibits the inhibitor. So if you inhibit DPP four effectively up regulates incretins which will cause an increase in incidence of these. Okay, now, So for nausea is such a glipizide, that's a, um, similar teo the A t t cell phone iron areas. Who caused the closure off? Um, the potassium channel which would cause depolarizations on the insulin release. Um, now, insulin is effectively a growth hormone, so this means that if you have high levels, it can lead to weight gain onda self and I areas because they act on this potassium channel because, um, a large increase in incident, then the other drugs have spoken about that. For that reason, Silvani areas a contraindication in obesity so glipizide would be contraindicated in obesity. Now moving on to metformin. This is the best drugs we have for treating type two diabetes on its first line. It reduces gluconeogenesis. Um and it does that by stopping the conversion off like lactate into glucose. Um, they also increases sensitivity and reduces absorption on have written here that it's contraindicated if the Jeffires less than 30. So this could be a problem if you have nephropat the and kidney disease as a result of your diabetes because metformin might be contraindicated blisters owns on work in a similar way. Such a period glitazone, which increases sensitivity on, um, contraindications. Heart failure. No. Yeah, ST t two inhibitors. So the's stop the re uptake off glucose from your kidneys, and as a result, glucose is excreted in your urine. Now, this is good because it lowers your blood placates. It can be bad, because if you have increased glucose in your urine, then you end up being at risk to ut eyes on thrush. Um, because on the glucose in the urine has good means. Glucose in, um, your urine tract say you end up providing that a food supply for bacteria to the thrive. Okay, now just his his a diagram that think knish made from us Keesey, which I thought really provided a good, um, get summary for the drugs that I just listed. But, um, Sahan a did mention this, but just I thought I mentioned c peptide on, um, insulin. So if you have in, it's in an OMA. Then you end up with increased C peptide because your body is producing the insulin. If you get access insulin from an injection and you have low C peptide on, this is just next on proof why c peptide could be useful and deciding what causes the hyperglycemia and then hypoglycemic. Uncalled symptoms. Such confusion attacks here, painting and irritability. Okay, now, that concludes my second part of the lecture on. But I just move on now, Teo, the SBA is that we spoke about at the start. So I'll get to your mind. And then that's a Honda. Go through her. Yeah. So Right. Um, this question one, I think it might be in question. Been questioned. Five on the Yeah, on the POTUS stop. It's a A 55 year old women is recently diagnosed with diabetes. She has a past history or systemically pissed. Um, erythematosus on chronic kidney disease within ETF are 35 and she has been my off that too. Which of the following drugs of contraindicators. Okay, I was just thinking, Sana because we did the polar start. Would it be better if you did your questions and then over Got those? Do the pool again now? Okay. Before you put the answer into the chapped, we're gonna do the pole again. Now, Teo, helpfully see if you improved and learn things over the course of the lecture. A complete know the answer is yes. And I have to open my presentation. Okay. Yeah, I'm sorry. That's my card. I opened my presentation because it has all the SBA options. Second, no worries. Okay, you know. Okay, So this was the first question. So we launched the pool again. Now, uh, yeah. Oh, yeah. Okay. Mazing is the first question of getting going to spend about 20 to 30 seconds. Um, on this. Uh huh. I take pictures of the owners of the ends. Also just a note for everybody I've popped The feedback form in the chat would really appreciate If you fill that out, you can get the slides, the recording. And also, in the next few days, you'll be getting some extra questions as well on a cheat sheet. We don't really appreciate if in the feedback Can you just tell us what you think of this new format with the questions at the beginning and the end? Did you feel it work? Did you feel it didn't on? Do you use that cream for my future sessions? Thank you. Okay, um, let me know at the end if you want me to go back to any question. Yeah. Yeah. Last one. Okay. If you want to go back to any question, that would be a good time to tell me. Taken crack on with the answers. Yeah. Question six. Okay. We had about 40% of you respond the last time. So it would be incredible if that many of you could respond again. Please. Questions. It's different. The pole. Okay, Which ones? Question six. Ah, If you open the polio area, this one is questions. Six. Okay, because the answer, because we haven't shared them yet. Give me a second. Okay. Give it another like 30 seconds. 78. The Yes. Okay. I'm gonna call the pole in about 15 seconds, so no. Okay. Right. Amazing. Thank you for answering, guys. You know, I'm gonna quick, please take photos of the results again. You can see the myself. Um um was done. Okay. Amazing. Great. So if I were to compare and arbitrate question if you question eight, for example, Initially, um, initially, how many of you got it? Dried out. See, um, initially, 31% of you got it, right. But now, after a presentation to 58% of you got a dry, it's that's really promising. Uh, yeah. Anyway, so, yeah, once. Once the game. Fine. So I was gonna go with the answers. Now, um, you don't have any questions after that, is no. Okay, go. Um, it's gonna go. Teo Toby's presentation. Uh huh. Okay. Yeah, that right. So this question, a 43 year old woman presents the emergency department with double vision and experiencing episodes of syncope. She also complains about feeling lethargic and has noticed that her clothes fit tight over the last few months off blood glucose reading shows that she's hypoglycemic. Which of the following blood markers is just that she has an incidentaloma. The correct answer is CPAP size Onda. This goes back to the physiology behind CPAP side. When you sense less insulin, you all to synthesize an equal concentration of CPAP tried. Therefore, if someone has a cancer which is releasing a lot of insulin which called insulin oma, then they're going to have raised C peptide, which correlates with raised insulin. Which of the following tissues have a high it can glue transporter. Uh, the correct answer to this was liver, punkers and kidneys. If you remember how high km means the low affinity, which means it takes a really large concentration of glucose for these tissues to open their Glucotrol glute two transporters. So the liver, pancreas and kidneys that are involved with metabolic SSM off Lucas Infed state on will only open the glue transporters at a high level of glucose. Um, that's the theory behind that. During pregnancy, women develop is in resistance. What home One is responsible for this change at us question earlier, the answer is HPLC, which is human percent elected in on this induces it was released from the placenta and induces incident resistance in the mother on this allows redirection off you close to the fetus. So congrats on become human on. But this one is a 46 year old woman with hypercholesterolemia and hypertension. And she was, It's a GP for a routine check up. She says she's noticing chest pain when she goes in the morning jogs but otherwise feels well. It's part of the routine work up of blood Glucose is done. A random glucose reading is 16.1 minimal Small eater. What is the next most appropriate step in management, given Sweeting. So the way I mean his question was to kind of put you off by giving the context of, like, something more cardiac that she's come in with like angina and give you a blood glucose results and see what you've done. So if we work through the options, the first one a prescribe metformin sulfonylurea. I'm those, uh, that those are medical pharmacological management options with that diabetes. But, um, you would not prescribe them here because you haven't technically diagnosed her yet officially, and if you did, the combination of metformin plus off longer is not first line. You would give metformin on his own first. Which leads me to be prescribed metformin. You haven't diagnosed her with diabetes yet. Um, and therefore you can't give him a foreman. I'll explain why in a second you can reassure them and send them home because 16.1 minimal is like significantly high and concerning and should be dealt with, UM, de no rapid insulin pens. You can't manage them with insulin injections just yet, because again, you haven't diagnosed on the insulin. She has no symptoms off things like DKA that require to give it give you any kind of insulin in the first place, so that would not be appropriate. The correct answer is we repeated test another day. This woman is common with symptoms that are related, angina and not diabetes, and therefore she's considered a symptomatic in the context of a blood glucose on their four. In order to diagnose and asymptomatic personal diabetes, you have to repeat the readings twice on separate occasions, and once you do diagnosed, you can prescribe incident. You can prescribe metformin if that's indicated or insulin injections, and that's indicated, Um, and that's why I use the correct answer. Come the lot of mine I'm gonna pause it with Toby now. Yeah, it's spotting. No. Okay, because yours no. Okay, presented you. It's a 55 year old. Women is recently diagnosed with diabetes. I spent I said this question area. Um, she has a past history of SLE and chronic kidney disease with an e g f r of 35. She's a B m i t. Which of the following drugs is contra indicated? Yeah. Say, um, glipizide is contraindicated on. I will explain why on this quite hard question, because the e jafar could throw you off. I say, um, s a director side is, um, a self diarrhea on it Causes increase. Um, insulin release on their four. Um, it can cause a B city on. Um, we don't want this to get any worse, So it's contraindicated in a beastie, and this lady has a very high B m i fitzer in the obese category. Now, you might have thought the answer was metformin because of the kidney disease, But actually, this is stage four kidney disease with an e jafar of 35. But you actually need the e jafar to be lower from that. For men to be contraindicated on this. Um, and this is why so metformin prevents the conversion of lactate to blue coast. So if you have lactate build up and then you get metabolic acidosis on if you're a Jeffires too low, then your kidneys can't remove this lactate. So and it will remain. Um, Andi, you end up with more severe metabolic acidosis. But in this case, the Jeffires greater than 30. So it's not contraindicated. Okay, next question. Um, 15 year old girl percents were really really nausea and vomiting. Um, on her key times a three on hepatitis C, um is for she treated for DKA. Which treatment is given, say the answers. Insulin, fluids and potassium. Um, again, this is hard because the potassium is four, which is actually a normal range. But when you give the insulin, the potassium is likely to drop, um, on. As a result, she is likely to need a testament fusion. Um, so that's why I passed him. Is the answer on do or say none of the other answers would be appropriate because housing click night, um, is used to stabilize the membrane and patients you have hyper clean. Yeah, on this patient does not have hyper cream here. Okay, that's hype on diabetic is very ill. He's read about diabetic sick rules, which actually actually take, um so he could increase insulin decrease insulin stop. Um, half is that form and days on one of their ketone is John says, increase insulin. Sorry. So you should increase his insulin. Because when you're ill, um, your body produces more glucose because you're you need the energy to help fight the infection. So as a result, you need more insulin both to know your blood glucose, but also help your body's uptake. Um, Theglobe case intercept the cells so they have energy to help fight the infection. Yeah. Okay. Um, but say that concludes our presentations. Raising, uh, thank you for coming and listening to us. Talk on D. Um, Booth, I see that about former certainly being posted, so it would be great if you could fill out that out for us so we can help. Pretty high teaching. If you got any questions, please put in the chat. Now we're happy to answer them out loud. I was gonna go over questions as previously, if you want already answered, uh, essentially privately. Very just a plug. Please, please do it. Then try Considerate. And the midsection next state on. Don't get a job. It's on cardiology. And, um, Tzakis is going to take us through a case scenario that don't have lots of twists and turns, and he's going to be drawing all over. His white board threw the recession. So if interested in interacting, asking him questions, Um, possibly getting to know them. Also feel free to attend. It's It's on our Facebook page, instagram everything so.